ESC Heart Failure最新文献

{"title":"Raising the Bar: Age-adjust NT-proBNP to improve specificity and reduce delay.","authors":"Lisa J Anderson","doi":"10.1002/ehf2.15427","DOIUrl":"https://doi.org/10.1002/ehf2.15427","url":null,"abstract":"","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel mutation associated with non-compaction ventricular myocardium: A case report.","authors":"Yan Li, Xi Wang, Saiyong Chen, Chun Wu, Fushi Piao","doi":"10.1002/ehf2.15403","DOIUrl":"https://doi.org/10.1002/ehf2.15403","url":null,"abstract":"","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to 'Frailty determinants in heart failure: inflammatory markers, cognitive impairment and psychosocial interaction'.","authors":"","doi":"10.1002/ehf2.15428","DOIUrl":"https://doi.org/10.1002/ehf2.15428","url":null,"abstract":"","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiometabolic outcomes with dapagliflozin after myocardial infarction by baseline ejection fraction: DAPA-MI.","authors":"David Erlinge, Stefan James, John Deanfield, Niclas Eriksson, Mark de Belder, Monér Alchay, David Austin, Daniel A Jones, Annica Ravn-Fischer, Sofia Sederholm Lawesson, Nikunj Shah, Julian W Strange, Karolina Szummer, Wilhelm Ridderstråle, Ehsan Parvaresh Rizi, Anna Maria Langkilde, Peter A Johansson, Darren K McGuire, Jonas Oldgren, Robert F Storey","doi":"10.1002/ehf2.15420","DOIUrl":"https://doi.org/10.1002/ehf2.15420","url":null,"abstract":"<p><strong>Aims: </strong>In the randomized DAPA-MI clinical trial, 10 mg of dapagliflozin once daily improved cardiometabolic outcomes versus placebo after acute myocardial infarction (MI) in patients without established diabetes or heart failure (HF). We assessed associations between baseline left ventricular ejection fraction (LVEF) and cardiometabolic outcomes in DAPA-MI.</p><p><strong>Methods: </strong>The primary outcome, assessed using the win ratio method, was the hierarchical composite of death, hospitalization for HF, non-fatal MI, atrial fibrillation/flutter, Type 2 diabetes, New York Heart Association classification at last visit and body weight decrease of ≥5% from baseline to last visit. For the present analysis, patients were categorized using LVEF at randomization (<50% or ≥50%).</p><p><strong>Results: </strong>Of the DAPA-MI participants with available LVEF data who received ≥1 dose of study drug (n = 3751), 2913 (77.7%) had LVEF <50% and 838 (22.3%) had LVEF ≥50%. The primary hierarchical composite outcome resulted in a win ratio favouring dapagliflozin of 1.38 (95% CI: 1.21, 1.57; P < 0.001) in patients with LVEF <50% and 1.32 (1.00, 1.73; P = 0.048) in patients with LVEF ≥ 50% (P interaction = 0.76). In a sensitivity analysis excluding patients with LVEF <30%, the primary hierarchical composite outcome resulted in a win ratio favouring dapagliflozin of 1.40 (95% CI: 1.22, 1.61; P < 0.001). There were no significant interactions between baseline LVEF and any secondary outcomes.</p><p><strong>Conclusions: </strong>Regardless of baseline LVEF, dapagliflozin resulted in significant cardiometabolic benefits versus placebo, although there was no impact on the composite of cardiovascular death or hospitalization for HF.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galectin-3 and kidney function in type 2 diabetes treated with dapagliflozin: Analysis from DECLARE-TIMI 58.","authors":"Paul M Haller, Stephen D Wiviott, David D Berg, Petr Jarolim, Erica L Goodrich, Deepak L Bhatt, Ingrid Gause-Nilsson, Lawrence A Leiter, Darren K McGuire, John P H Wilding, Itamar Raz, Marc S Sabatine, David A Morrow","doi":"10.1002/ehf2.15415","DOIUrl":"https://doi.org/10.1002/ehf2.15415","url":null,"abstract":"<p><strong>Background: </strong>Galectin-3 (Gal-3) is a circulating biomarker of fibrosis, with higher levels being associated with an increased risk of progression of heart failure and kidney disease. Patients with type 2 diabetes mellitus (T2DM) are at increased risk of both.</p><p><strong>Methods: </strong>DECLARE-TIMI 58 was a randomized, placebo-controlled trial of dapagliflozin in patients with T2DM with or at high risk for atherosclerotic cardiovascular disease and creatinine clearance ≥60 mL/min. In a nested biomarker substudy, Gal-3 was measured at baseline and in adjusted analyses associated with the prespecified kidney-specific composite endpoint [Kidney-EP; sustained ≥40% decrease in estimated glomerular filtration rate (eGFR) to <60 mL/min, new end-stage kidney disease or adjudicated kidney-related death].</p><p><strong>Results: </strong>Among 14 530 pts, median Gal-3 was 14.9 ng/mL [interquartile range (IQR), 11.9, 18.4]. Gal-3 was weakly associated with urine albumin creatinine ratio (r = 0.098, P < 0.0001) and eGFR (r = -0.27, P < 0.001) at baseline and independently associated with the Kidney-EP:adj hazard ratio (HR) 1.15 [95% confidence interval (CI) 1.03, 1.28] per 1-SD log (Gal-3), P = 0.013. Dapagliflozin significantly reduced the relative risk of the Kidney-EP across quartiles of baseline Gal-3 [overall HR 0.45 (95% CI 0.23, 0.85), P < 0.0001; P interaction = 0.87]. A greater risk difference was observed with dapagliflozin in patients with higher Gal-3, in whom a higher absolute risk at baseline was observed [absolute risk reduction (ARR) Q4 1.9 (95% CI 0.6, 3.2) vs. Q1 0.6% (-0.1, 1.3), ARR P trend 0.048].</p><p><strong>Conclusions: </strong>Plasma Gal-3 is independently associated with the progression of kidney dysfunction in patients with T2DM and normal kidney function. There was a gradient of greater absolute benefit for reducing kidney disease progression in patients treated with dapagliflozin and with higher Gal-3 concentrations at baseline, in whom a higher absolute risk was observed.</p><p><strong>Registration: </strong>clinicaltrials.gov (NCT01730534).</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Empagliflozin after myocardial infarction with or without diabetes and chronic kidney disease: Insights from EMPACT-MI.","authors":"Francesco Fioretti, Javed Butler, Jacob A Udell, W Schuyler Jones, Mark C Petrie, Josephine Harrington, Michaela Mattheus, Johann Bauersachs, Antoni Bayes-Genis, Shaun G Goodman, Tomasz Gasior, James L Januzzi, Renato D Lopes, Piotr Ponikowski, Xavier Rossello, Morten Schou, Peter van der Meer, Dragos Vinereanu, Shelley Zieroth, Martina Brueckmann, Mikhail Sumin, Deepak L Bhatt, Adrian F Hernandez, Stefan D Anker","doi":"10.1002/ehf2.15393","DOIUrl":"https://doi.org/10.1002/ehf2.15393","url":null,"abstract":"<p><strong>Background: </strong>In the EMPACT-MI trial, empagliflozin did not reduce the primary endpoint of all-cause mortality or hospitalization for heart failure (HHF) following acute myocardial infarction (AMI) but was associated with a risk reduction for HF events.</p><p><strong>Objectives: </strong>This study aimed to evaluate whether the effect of empagliflozin on HF events is consistent in patients with and without type 2 diabetes and/or chronic kidney disease enrolled in the EMPACT-MI trial.</p><p><strong>Methods: </strong>Post hoc analysis assessing the effect of empagliflozin on the primary endpoint and on HF events in AMI patients with and without an established recommendation for a sodium-glucose cotransporter-2 inhibitor (SGLT2i) (type 2 diabetes or chronic kidney disease).</p><p><strong>Results: </strong>Of 6522 participants, 3489 (53%) did not have type 2 diabetes and/or chronic kidney disease. Those without these conditions were younger and with fewer comorbidities. No differences were observed for the primary endpoint. Empagliflozin reduced time to first HHF, total HHF, time to adverse event (AE) of HF (including outpatient HF events) and total AEs of HF similarly in patients with and without type 2 diabetes or chronic kidney disease. Total HHFs were 50 and 63 [adjusted event rate 1.74 and 2.31 events per 100 patient-years; rate ratio (RR) 0.75; 95% confidence interval (CI) 0.48, 1.18] in patients without and 98 and 144 (adjusted event rate 3.91 and 6.04 events per 100 patient-years; RR 0.65; 95% CI 0.45, 0.94; P for interaction = 0.61) in those with type 2 diabetes or chronic kidney disease in the empagliflozin and placebo arms, respectively. Any AEs, serious AEs and AEs leading to permanent study drug discontinuation were similar between treatment groups in both subgroups.</p><p><strong>Conclusions: </strong>Empagliflozin improved HF outcomes similarly in patients after AMI with or without type 2 diabetes or chronic kidney disease.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary artery compliance in aortic stenosis: protective or maladaptive? Rethinking the conclusions on PAPi prognostic value.","authors":"Shichen Hu, Hong Zhou","doi":"10.1002/ehf2.15429","DOIUrl":"https://doi.org/10.1002/ehf2.15429","url":null,"abstract":"","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145052046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epidemiology, pathophysiology, diagnosis and management of atrial functional mitral regurgitation: An expert opinion paper.","authors":"Matteo Pagnesi, Mauro Riccardi, Francesco Maisano, Julia Grapsa, Vassilis Barberis, Magdy Abdelhamid, Elena-Laura Antohi, Henrike Arfsten, Nicole Karam, Denisa Muraru, Karl-Philipp Rommel, Anna Sannino, Wilfried Mullens, Marianna Adamo, Marco Metra","doi":"10.1002/ehf2.15405","DOIUrl":"https://doi.org/10.1002/ehf2.15405","url":null,"abstract":"<p><p>Atrial functional mitral regurgitation (AFMR) is an increasingly recognized subtype of mitral regurgitation, characterized by left atrial remodelling and mitral annular dilation in the absence of primary mitral valve disease or left ventricular dysfunction. Closely linked to chronic atrial fibrillation and heart failure with preserved ejection fraction, AFMR is associated with poor clinical outcomes and represents a growing therapeutic challenge. This expert opinion paper summarizes current evidence on the epidemiology, pathophysiology, diagnosis and management strategies, including medical therapy and emerging data supporting surgical and transcatheter interventions in selected patients. However, data from prospective controlled clinical trials are still lacking. Future research is needed to refine patient selection, long-term outcomes and to support evidence-based recommendations for this increasingly prevalent condition.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"First evaluation of a novel pulsatile LVAD: Feasibility and haemodynamic impact in acute heart failure.","authors":"Sara Knigge, Marcelo B Bastos, Bastian Schmack, Liam Schana, Oren Malchin, Ali S Merzah, Aron F Popov, Alexander Weymann, Arjang Ruhparwar, Felix Schumacher, Günes Dogan, Jan D Schmitto","doi":"10.1002/ehf2.15410","DOIUrl":"https://doi.org/10.1002/ehf2.15410","url":null,"abstract":"<p><strong>Aims: </strong>Non-pharmacological therapies for acute decompensated heart failure (HF) and cardiogenic shock have evolved considerably in recent decades. Short-term mechanical circulatory support (MCS) devices can be used as circulatory backup. While nearly all available devices use continuous flow, evidence indicates that pulsatile flow can be more effective. This study presents the first experimental use of a novel counter-pulsatile left ventricular (LV) assist device (LVAD) with a primary focus on assessing its feasibility and effectiveness.</p><p><strong>Methods: </strong>The pulsatile ventricular assist platform (pVAP) was applied in six porcine models of acute ischaemic HF with the inlet in the left atrium and the outlet in the aorta. HF was induced through stepwise ligation of the left anterior descending artery and its diagonal branches. The pVAP functioned driven by a conventional IABP console while LV pressure-volume (PV) loops and standard haemodynamics with the device OFF and ON were recorded. Absolute values and percent variations were compared using Mann-Whitney's U test and Wilcoxon's sign-rank test.</p><p><strong>Results: </strong>The device's output flow is frequency dependent, with an output flow of 2.64 ± 0.22 L/min at 80 bpm. Activation reduced the EDV [132 (90-145) vs. 118 (83-130) mL, P < 0.05], EDP 9 (6-10) vs. 6 (5-9) mmHg, P < 0.001], native cardiac output [CO_N, 3.64 (2.88-6.71) vs. 1.67 (1.24-2.48) L/min, P < 0.001] and myocardial oxygen consumption [pressure-volume area * heart rate (PVA*HR), 4592 (2944-9272) vs. 2901 (1915-4437) mJ, P < 0.001]. Contractility decreased, with right-shifting the end-systolic PV relationship (ESPVR) while ESP and forward cardiac output CO_F were constant. The mean arterial pressure increased [54 (48-60) vs. 49 (42-55) mmHg, P < 0.001] and mPAP decreased [10 (8-11) to 9 (7-10) mmHg, P < 0.01]. The PV loop shifted left and downward. No changes occurred in the passive-elastic properties of the LV in diastole.</p><p><strong>Conclusions: </strong>The pVAP reduced the LV mechanical load while increasing systemic pressures and reducing pulmonary pressures. Its functionality as an LVAD is characterised by consistent and predictable performance. Further research is necessary to elucidate the physiological and clinical impact of the device in animals and, subsequently, in humans.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of Nrf2 in heart failure: From cardioprotection to therapeutic approaches.","authors":"Emiliano Fiori, Sergio Davinelli, Armando Ferrera, Alessandro Medoro, Carlo Barsali, Allegra Battistoni, Maurizio Volterrani, Massimo Volpe, Luciano Saso, Speranza Rubattu","doi":"10.1002/ehf2.15406","DOIUrl":"https://doi.org/10.1002/ehf2.15406","url":null,"abstract":"<p><p>Heart failure (HF) is a multifactorial and pathophysiological complex syndrome, involving not only neurohormonal activation but also oxidative stress, chronic low-grade inflammation, and metabolic derangements. Central to the cellular defence against oxidative damage is nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that orchestrates antioxidant and cytoprotective responses. Preclinical in vitro and in vivo studies reveal that Nrf2 signalling is consistently impaired in HF, contributing to the progression of myocardial dysfunction. The loss of Nrf2 activity intersects a complex network of pathological processes involving neurohormonal activation, ischaemia-reperfusion injury, and sustained inflammation, exacerbating cardiac functional decline. Nrf2 deficiency diminishes resilience to clinical conditions such as hypertension, diabetic cardiomyopathy, and cancer therapy-related cardiotoxicity, favouring the transition from initial cardiac dysfunction to overt HF. Initial evidence supports the therapeutic potential of Nrf2 modulation. Lifestyle interventions such as exercise training, various natural compounds, and established cardiovascular agents (e.g. sodium-glucose cotransporter-2 inhibitors) have been shown to restore Nrf2 activity. This review analyses the emerging role of Nrf2 as both a key player in HF pathogenesis and a promising therapeutic target, highlighting available evidence across HF phenotypes and addressing the controversies surrounding its pharmacological modulation.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}